Key result
Allocryptopine reduces transmural dispersion of repolarization by ~45% in rabbit ventricular myocardium.
Why the study?
Does allocryptopine affect outward potassium current and slow delayed rectifier potassium current in rabbit myocardium?
Does allocryptopine affect outward potassium current and slow delayed rectifier potassium current in rabbit myocardium?
Allocryptopine reduces transmural dispersion of repolarization by inhibiting outward potassium current and slow delayed rectifier potassium current in rabbit myocardium, providing a potential mechanism for its anti-arrhythmic effects.
May indicate anti-arrhythmic potential via potassium currents in rabbits; leaves open translation to human arrhythmia therapy.
OBJECTIVE: Allocryptopine (ALL) is an effective alkaloid of Corydalis decumbens (Thunb.) Pers. Papaveraceae and has proved to be anti-arrhythmic. The purpose of our study is to investigate the effects of ALL on transmural repolarizing ionic ingredients of outward potassium current (I to) and slow delayed rectifier potassium current (I Ks). METHODS: The monophasic action potential (MAP) technique was used to record the MAP duration of the epicardium (Epi), myocardium (M) and endocardium (Endo) of the rabbit heart and the whole cell patch clamp was used to record I to and I Ks in cardiomyocytes of Epi, M and Endo layers that were isolated from rabbit ventricles. RESULTS: The effects of ALL on MAP of Epi, M and Endo layers were disequilibrium. ALL could effectively reduce the transmural dispersion of repolarization (TDR) in rabbit transmural ventricular wall. ALL decreased the current densities of I to and I Ks in a voltage and concentration dependent way and narrowed the repolarizing differences among three layers. The analysis of gating kinetics showed ALL accelerated the channel activation of I to in M layers and partly inhibit the channel openings of I to in Epi, M and Endo cells. On the other hand, ALL mainly slowed channel deactivation of I Ks channel in Epi and Endo layers without affecting its activation. CONCLUSIONS: Our study gives partially explanation about the mechanisms of transmural inhibition of I to and I Ks channels by ALL in rabbit myocardium. These findings provide novel perspective regarding the anti-arrhythmogenesis application of ALL in clinical settings.
No takes yet. Share an insight, caveat, or question.
Fu et al. (2016) studied Normal rabbit myocardium (n=12). Allocryptopine vs. Baseline/Control was evaluated on Transmural dispersion of repolarization (TDR) in ms (p=<0.01). Allocryptopine significantly reduced the transmural dispersion of repolarization in rabbit ventricular myocardium from 29.5 ms to 16.2 ms.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: